Lack of First Phase Insulin Response in TD Subjects

Besides the reduced insulin-mediated glucose uptake in skeletal muscle (and in liver and fat tissue), the abnormal insulin secretion pattern characterised by a lack of first-phase insulin release may also play a pathophysiological role, since the postprandial insulin peaks disappear in T2D subjects (Fig. 3). A recent publication has shown that the reduction of the first-phase insulin response to meals is already present at normal fasting glucose values in T2D subjects [13]. This indicates a need for an earlier insulin treatment than what has been the routine for several years. Furthermore, these findings indicate that it is unphysiological to treat

Control group Triple therapy group

18 24 Time

14 12

500r

"55 400

"is

Endogenous sulin Insulin Aspart

18 24 Time

14 12

Control group Triple therapy group

Control group Triple therapy group

Time

Fig. 3. Twenty-four-hour blood glucose (a) and insulin (b) values together with insulin aspart values (c) after 6 months of treatment with either NPH insulin (control group) or triple therapy. (d) The scattered area represents the 24-h insulin profile in healthy non-diabetic subjects in hospital. Eight-point home-measured blood glucose profiles in all subjects studied (mean values) [17].

T2D subjects with NPH (Neutral Protamine Hagedorn) insulin once or twice daily, as it only increases the 24-h plasma insulin values without reconstructing the physiological insulin profile. However, the insulin response to meals can be reconstructed using rapid-acting insulin analogues. Therefore, based on this pathophysiological consideration, it is difficult to find the arguments for the present routine with NPH insulin or long-acting insulin analogues once or twice daily, without treating postprandial hyperglycaemia.

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